Search results for " Lymphocyte Activation"

showing 8 items of 8 documents

The transcription factor NFATc2 controls IL-6–dependent T cell activation in experimental colitis

2008

The nuclear factor of activated T cells (NFAT) family of transcription factors controls calcium signaling in T lymphocytes. In this study, we have identified a crucial regulatory role of the transcription factor NFATc2 in T cell–dependent experimental colitis. Similar to ulcerative colitis in humans, the expression of NFATc2 was up-regulated in oxazolone-induced chronic intestinal inflammation. Furthermore, NFATc2 deficiency suppressed colitis induced by oxazolone administration. This finding was associated with enhanced T cell apoptosis in the lamina propria and strikingly reduced production of IL-6, -13, and -17 by mucosal T lymphocytes. Further studies using knockout mice showed that IL-…

Adjuvants Immunologic; Animals; Humans; Interleukin-13; Interleukin-17; Interleukin-6; Lymphocyte Activation; Mice; Mice Inbred BALB C; Mice Knockout; Mice SCID; Models Biological; NFATC Transcription Factors; Oxazolone; T-LymphocytesT cellT-LymphocytesImmunologyMice SCIDBiologyLymphocyte ActivationInflammatory bowel diseaseModels BiologicalArticleOxazoloneTCIRG1chemistry.chemical_compoundMiceAdjuvants ImmunologicmedicineImmunology and AllergyCytotoxic T cellAnimalsHumansColitisMice KnockoutMice Inbred BALB CInterleukin-13NFATC Transcription FactorsInterleukin-6Interleukin-17OxazoloneArticlesmedicine.diseasemedicine.anatomical_structurechemistryImmunologyInterleukin 13Cancer researchInterleukin 17The Journal of Experimental Medicine
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Missense mutations in the fas gene resulting in autoimmune lymphoproliferative syndrome: A molecular and immunological analysis

1997

AbstractProgrammed cell death (or apoptosis) is a physiological process essential to the normal development and homeostatic maintenance of the immune system. The Fas/Apo-1 receptor plays a crucial role in the regulation of apoptosis, as demonstrated by lymphoproliferation in MRL-lpr/lpr mice and by the recently described autoimmune lymphoproliferative syndrome (ALPS) in humans, both of which are due to mutations in the Fas gene. We describe a novel family with ALPS in which three affected siblings carry two distinct missense mutations on both the Fas gene alleles and show lack of Fas-induced apoptosis. The children share common clinical features including splenomegaly and lymphadenopathy, b…

Antigens Differentiation T-LymphocyteMaleAdolescentT-LymphocytesCD3ImmunologyLymphoproliferative disordersBiologyLymphocyte ActivationAutoimmune DiseaseBiochemistryFas ligandImmunophenotypingImmune systemPedigree; Antigens Differentiation T-Lymphocyte; Solubility; Apoptosis; Autoimmune Diseases; Humans; Antigens CD95; Child; Lymphocytes; Child Preschool; Lymphocyte Activation; Syndrome; Lymphoproliferative Disorders; Adolescent; Mutation; Immunophenotyping; Male; Biological Markers; T-LymphocytesmedicineChildAutoimmune diseaseApoptosiSyndromeCell BiologyHematologymedicine.diseaseFas receptorPedigreeAntigens CD95SolubilityApoptosisChild PreschoolLymphoproliferative DisorderAutoimmune lymphoproliferative syndromeMutationBiological MarkerImmunologybiology.proteinLymphocyteHuman
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Potential involvement of IL-9 and Th9 cells in the pathogenesis of rheumatoid arthritis

2015

Objective IL-9 has been shown to be upregulated before the clinical onset of articular disease in RA. The exact role of IL-9 and Th9 cells in RA, however, has not yet been adequately studied. The aim of this study was to evaluate the expression of IL-9 and IL-9-expressing cells in RA patients. Methods IL-9, IL-9R, PU.1, IL-9, thymic stromal lymphopoietin (TSLP), IL-4 and TGF-β expression was assessed by real-time-PCR in the synovial tissues of RA and OA patients. IL-9, IL-9R, IL-4, TSLP and TGF-β were also investigated by immunohistochemistry. Peripheral CD4(+) T cell subsets were studied by flow cytometry analysis before and after incubation with citrullinated peptides. Results IL-9 was ov…

CD4-Positive T-LymphocytesMaleCitrullinated peptide; IL-9; Rheumatoid arthritis; Th9 cells; Adolescent; Adult; Arthritis Rheumatoid; CD4-Positive T-Lymphocytes; Cells Cultured; Cytokines; Female; Gene Expression Regulation; Humans; Interleukin-4; Interleukin-9; Lymphocyte Activation; Male; Middle Aged; RNA Messenger; Synovial Membrane; T-Lymphocyte Subsets; Transforming Growth Factor beta; Young Adult; Rheumatology; Medicine (all); Pharmacology (medical)MessengerLymphocyte ActivationArthritis RheumatoidT-Lymphocyte SubsetsTransforming Growth Factor betaRheumatoidTh9 cellPharmacology (medical)Cells CulturedCulturedmedicine.diagnostic_testbiologyMedicine (all)Synovial MembraneMiddle Agedmedicine.anatomical_structureCD4-Positive T-LymphocyteCytokinesFemaleArthritiHumanAdultThymic stromal lymphopoietinAdolescentT cellCD3T-Lymphocyte SubsetCitrullinated peptidePeripheral blood mononuclear cellFlow cytometryYoung AdultRheumatologyThymic Stromal LymphopoietinmedicineHumansInterleukin 9RNA MessengerCytokineInterleukin 4Rheumatoid arthritibusiness.industryInterleukin-9IL-9Settore MED/16 - ReumatologiaGene Expression RegulationImmunologybiology.proteinRNACellInterleukin-4Synovial membranebusiness
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CD4+CD25+ regulatory T cells inhibit natural killer cell functions in a transforming growth factor-beta-dependent manner.

2007

Tumor growth promotes the expansion of CD4+CD25+ regulatory T (T reg) cells that counteract T cell–mediated immune responses. An inverse correlation between natural killer (NK) cell activation and T reg cell expansion in tumor-bearing patients, shown here, prompted us to address the role of T reg cells in controlling innate antitumor immunity. Our experiments indicate that human T reg cells expressed membrane-bound transforming growth factor (TGF)–β, which directly inhibited NK cell effector functions and down-regulated NKG2D receptors on the NK cell surface. Adoptive transfer of wild-type T reg cells but not TGF-β−/− T reg cells into nude mice suppressed NK cell–mediated cytotoxicity, redu…

MESH : CytokinesMESH: Flow CytometryMESH : Immunity NaturalMESH: T-LyLymphocyte ActivationT-Lymphocytes RegulatoryMiceInterleukin 210302 clinical medicineT-Lymphocyte SubsetsTransforming Growth Factor betaNeoplasmsMESH : Receptors ImmunologicMESH : Cell ProliferationImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyMESH: AnimalsMESH: NeoplasmsIL-2 receptorReceptors Immunologic0303 health sciencesMESH: Cytokineshemic and immune systemsFlow CytometryNatural killer T cell3. Good healthCell biologyKiller Cells Naturalmedicine.anatomical_structureNK Cell Lectin-Like Receptor Subfamily KInterleukin 12CytokinesReceptors Natural Killer Cell[SDV.IMM]Life Sciences [q-bio]/ImmunologyFranceMESH : Killer Cells NaturalMESH : Cytotoxicity Tests ImmunologicMESH: Killer Cells NaturalMESH: Cell Line TumorMESH : Flow CytometryImmunologychemical and pharmacologic phenomenaMESH: Cytotoxicity Tests ImmunologicMESH : Mice Inbred C57BLBiologyArticleNatural killer cell03 medical and health sciencesMESH: Mice Inbred C57BLCell Line TumorMESH: Cell ProliferationMESH : MicemedicineAnimalsHumansAntigen-presenting cellMESH: Lymphocyte ActivationMESH : FranceMESH: MiceMESH: Receptors ImmunologicMESH : Lymphocyte ActivationCell Proliferation030304 developmental biologyMESH: Immunity NaturalLymphokine-activated killer cellMESH: HumansMESH : Cell Line TumorMESH : HumansCytotoxicity Tests ImmunologicNKG2DMESH : T-LyMESH : NeoplasmsImmunity InnateMice Inbred C57BLMESH: FranceMESH : Animals030215 immunology
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Effect of cytomegalovirus-induced immune response, self antigen-induced immune response, and microbial translocation on chronic immune activation in …

2013

International audience; We evaluated the impact of cytomegalovirus (CMV)-induced immune responses, autoimmune-induced immune responses, and microbial translocation on immune activation in 191 human immunodeficiency virus type 1-infected patients from the ANRS CO3 Aquitaine Cohort. All enrolled subjects had achieved long-term virological suppression during receipt of combination antiretroviral therapy (cART). HLA-DR(+)/CD38(+) expression was 16.8% among CD8(+) T cells. Independent of age, CD4(+) T-cell count, 16S ribosomal DNA load, and regulatory T-cell count, positive results of Quantiferon CMV analysis (P = .02), positive results of CMV-pp65 enzyme-linked immunosorbent spot analysis (P = …

MaleCytomegalovirusAutoimmunityHIV InfectionsCD8-Positive T-LymphocytesCD38Lymphocyte Activationmedicine.disease_causeAutoimmunityCohort Studies0302 clinical medicine[SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases[ SDV.MP ] Life Sciences [q-bio]/Microbiology and ParasitologyAntiretroviral Therapy Highly ActiveImmunology and Allergy030212 general & internal medicineMESH: Cytomegalovirus Infections/immunologyMESH: HLA-DR Antigens/metabolismMESH: Cohort Studies0303 health sciencesMESH: HIV Infections/drug therapyvirus diseasesViral Load3. Good healthInfectious Diseases[SDV.MP]Life Sciences [q-bio]/Microbiology and ParasitologyMESH: CD8-Positive T-Lymphocytes/immunologyCytomegalovirus Infections[SDV.MHEP.MI] Life Sciences [q-bio]/Human health and pathology/Infectious diseases[SDV.IMM]Life Sciences [q-bio]/ImmunologyFemaleFranceMESH: Cytomegalovirus/immunologyMESH: Viral Load[SDV.IMM] Life Sciences [q-bio]/ImmunologyCongenital cytomegalovirus infectionHuman leukocyte antigenBiologyQuantiFERONViral Matrix Proteins03 medical and health sciencesImmune systemMESH: Cross-Sectional StudiesAntigenMESH: AutoimmunitymedicineHumansMESH: Phosphoproteins/immunology[SDV.MP] Life Sciences [q-bio]/Microbiology and ParasitologyMESH: Viral Matrix Proteins/immunology030304 developmental biologyMESH: HumansMESH: HIV-1/geneticsMESH: HIV-1/physiologyMESH: HIV Infections/immunologyHLA-DR AntigensPhosphoproteinsmedicine.diseaseVirologyMESH: MaleMESH: Lymphocyte Activation/immunologyMESH: FranceCross-Sectional Studies[SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologieImmunologyHIV-1[SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologieMESH: HIV-1/drug effectsMESH: FemaleCD8
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Mast cells counteract regulatory T-cell suppression through interleukin-6 and OX40/OX40L axis toward Th17-cell differentiation

2009

Abstract The development of inflammatory diseases implies inactivation of regulatory T (Treg) cells through mechanisms that still are largely unknown. Here we showed that mast cells (MCs), an early source of inflammatory mediators, are able to counteract Treg inhibition over effector T cells. To gain insight into the molecules involved in their interplay, we set up an in vitro system in which all 3 cellular components were put in contact. Reversal of Treg suppression required T cell–derived interleukin-6 (IL-6) and the OX40/OX40L axis. In the presence of activated MCs, concomitant abundance of IL-6 and paucity of Th1/Th2 cytokines skewed Tregs and effector T cells into IL-17–producing T cel…

Regulatory T cellmedicine.medical_treatmentCellular differentiationImmunologyPriming (immunology)chemical and pharmacologic phenomenaMice TransgenicMast cell; T regulatory cell; Immune responseBiologyLymphocyte ActivationT-Lymphocytes RegulatoryBiochemistryImmune toleranceMiceMice CongenicmedicineImmune ToleranceMast CellT regulatory cellImmune responseCells CulturedCell ProliferationAnimalInterleukin-6Experimental autoimmune encephalomyelitisInterleukin-17hemic and immune systemsCell DifferentiationT lymphocyteT-Lymphocytes Helper-InducerHematologyCell BiologyReceptors OX40medicine.diseaseCell biologyMice Inbred C57BLmedicine.anatomical_structureCytokineImmunologyAnimals; Cell Differentiation; Cell Proliferation; Cells Cultured; Immune Tolerance; Interleukin-17; Interleukin-6; Lymphocyte Activation; Mast Cells; Membrane Glycoproteins; Mice; Mice Congenic; Mice Inbred C57BL; Mice Transgenic; Receptors OX40; Signal Transduction; T-Lymphocytes Helper-Inducer; T-Lymphocytes Regulatory; Tumor Necrosis Factors; Hematology; Biochemistry; Cell Biology; ImmunologyInterleukin 17Membrane GlycoproteinTumor Necrosis FactorSignal Transduction
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Synergistic effects of fluticasone propionate and salmeterol on in vitro T-cell activation and apoptosis in asthma

2004

Background In asthma T cells are characterized by an increased activation state and by reduced apoptosis. Objective Because the clinical efficacy of inhaled corticosteroids combined with long-acting β 2 -agonists has been widely demonstrated in asthma, we studied, in vitro , the effect of fluticasone propionate (FP) and salmeterol alone and in combination on the activation and apoptosis of peripheral blood T cells (PBTs), on the expression of phosphorylated nuclear factor κB inhibitor (IκBα), and on the nuclear translocation of glucocorticoid receptor (GR) in PBTs from asthmatic subjects. Methods Apoptosis was evaluated on the basis of annexin V binding, whereas the expression of caspases 8…

medicine.medical_specialtyProgrammed cell deathAdolescentT cellT-LymphocytesImmunologyActive Transport Cell NucleusApoptosisAndrostadienes; Active Transport Cell Nucleus; NF-kappa B; Apoptosis; Humans; Albuterol; Receptors Glucocorticoid; Asthma; Child; Caspases; Lymphocyte Activation; Phosphorylation; I-kappa B Proteins; Adolescent; Drug Synergism; T-LymphocytesLymphocyte ActivationGlucocorticoid receptorReceptors GlucocorticoidNF-KappaB Inhibitor alphaAnnexinInternal medicinemedicineHumansImmunology and AllergyAlbuterolPhosphorylationChildSalmeterol XinafoateAndrostadieneChemistryActive Transport Cell NucleuNF-kappa BApoptosiDrug SynergismCaspaseAsthmaAndrostadienesIκBαEndocrinologymedicine.anatomical_structureApoptosisCaspasesFluticasoneI-kappa B ProteinI-kappa B ProteinsSalmeterolGlucocorticoidmedicine.drugHuman
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Impact of Sars-CoV2 Infection on 491 Hematological Patients: The Ecovidehe Multicenter Study

2020

INTRODUCTION Coronavirus disease 2019 (COVID-19) caused by SARS-CoV2 virus is thought to be more severe in patients with prior hematological diseases. There is evidence suggesting that hematological patients are particularly vulnerable and have a higher risk of developing severe events, with higher mortality rate than general population. However, the available data are limited, and prognostic factors at admission still remain unclear. With this background, our aims were to analyze the impact of hematological diseases and their therapy on the COVID-19 severity and to identify clinical and biological risk factors to predict the outcome in these patients. METHODS We carried out a multicenter …

medicine.medical_specialtyeducation.field_of_studybusiness.industryMortality rateImmunologyPopulation203.Lymphocytes Lymphocyte Activation and Immunodeficiency including HIV and Other InfectionsRetrospective cohort studyCell BiologyHematologyDiseasemedicine.diseaseBiochemistryComorbidityMulticenter studyInternal medicineIntensive caremedicineIn patienteducationbusinessBlood
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